The Section conducts a wide range of research with a focus on the functions of the human prefrontal cortex, memory and amnesia, and cognitive neuroplasticity. We have continued to refine a model developed in the Section that specifies some of the characteristics of the prefrontal cortex's underlying cognitive architecture. We have determined that ease of access to knowledge stored in the prefrontal cortex is determined by the category and familiarity of that knowledge. In addition, failure to selectively retrieve such knowledge leads to impaired plan development and/or execution. Activating knowledge stored in prefrontal cortex allows for control processes to manage information that has to be kept temporarily active. We have also been able to measure the effects of meaningfulness, modality, and memory load of this temporarily active verbal and nonverbal information on brain activity using event-related potentials. We have also conducted a small set of studies to determine the types of binding that are spared and impaired in amnesia. Our results strongly indicate that binding between contextual information (perhaps stored in the prefrontal cortex) and more basic representational knowledge or surface features (perhaps stored in posterior cortex) is modulated by the hippocampus and related structures and can account for a wide range of memory failures in amnesic patients. Other research in the Section has indicated that brain structures complementary to the hippocampus are especially involved in encoding the emotional aspects of information. In an effort to better understand some aspects of cognitive neuroplasticity, we have examined the learning rate of patients recovering from brain damage and with deficits on the task of interest and compared their performance to matched controls. There is some indication that patients can show new learning in deficit areas but it is not clear that if new learning is without a cost to preserved cognitive functions. Our research ascertaining whether induced restrictions in stimulus processing via a particular sensory modality alters which circumscribed brain sectors are bracketed together for that particular functional purpose has not yet resulted in a clear finding. Our current work is analyzing whether, paradoxically under certain conditions, smaller brain lesions have a relatively greater negative effect on functional plasticity than relatively larger lesions.